Jean-Luc Puel started his scientific career in Montpellier in 1983 in the Inserm’s laboratory U254 (Laboratoire Neurobiologie de l'Audition) directed by Professor Rémy Pujol. In 1986, he defended his PhD thesis "frequency selectivity in rats during development and after ototoxic drugs administration" and joined Professor Richard P. Bobbin's laboratory (Department of Otorhinolaryngology, Louisiana State University, New-Orleans) as a post-doctoral fellow. During his postdoctoral training, he developed several research programs on the pharmacology of the cochlea. In 1989, he came back to France and was appointed as a researcher by the CNRS to develop pharmacological therapies of the inner ear. In 1998, Jean-Luc Puel became Director of Research at the CNRS. Later on, he obtained a position as Professor of Neuroscience at the University of Montpellier 1 and became director of the “Research centre for hearing aids” in 2001. During this period, he actively participated with Christian Hamel, Jean Valmier and Alain Privat to the creation of the Institute of Neurosciences of Montpellier. This institute, in which he managed the hearing team”, has been inaugurated in 2003. In 2011, he succeeded to Christian Hamel to head the Institute (INM-Inserm U1051).
Jean-Luc Puel's research interests are focused on the normal and pathological functioning of the inner ear. They include researches on the encoding of the sensory message and on the protection and regeneration of sensory epithelia in acquired genetic deafness. Interests are also oriented on tinnitus.
Logic of sound coding and tinnitus
Our former study demonstrated that glutamate is the neurotransmitter mediating fast synaptic transmission via AMPA-preferring receptors located the auditory nerve fibers (see Puel 1995 for review). Later on, we have identified SLC17A8, which encodes the vesicular glutamate transporter-3 (VGLUT3), as the gene responsible for nonsyndromic deafness DFNA25. We demonstrated that genetic deletion of Slc17a8 in mice results in a profound deafness because of the lack of glutamate release from the IHCs onto the auditory nerve fibers (Ruel et al., Am J Hum Genet. 2008). This synapse is tonically regulated by dopamine (Ruel et al., J Neurochem. 2006). Finally, we demonstrated in a behavioural animal model that tinnitus resulted from “abnormal” activation of NMDA receptors (Guitton et al, J. Neurosci. 2003). Targeting cochlear NMDA receptors may present a promising strategy to treat tinnitus (Ruel et al., J. Neurosci. 2008).
Degeneration and protection of the cochlea
The auditory sensory cells are vulnerable to a variety of exogenous factors such as loud noise, aminoglycoside antibiotics and antimitotic drugs. We have previously shown that the mitochondrial pathway is extensively activated in cells in response to extracellular signals and internal insults (e.g. DNA damage), and thus designed therapeutic strategies to rescue the cochlea after noise using local applications of specific peptide inhibitors of JNK, caspases or calpains (Wang and Puel, Mini Rev Med Chem. 2008 ). Our interest are now extend to age-related-hearing loss (Menardo et al, Antioxid Redox Signal. 2012)
To promote clinical transfer, we collaborate with Big Pharma (Sanofi) and Industrial companies (Cochlear®, Neurelec®, Entendre). The output of our researches is the development of a totally implantable inner ear drug delivery device to treat deafness and tinnitus. This project called SAMI (Santé, Audition, Microsystème Implantés) is supported by the ITMO technologies for health.
Bibliography (h index = 36)
113 publications (3291 Citations, Average per Item 29.12)
4 patents (WO 2004/02206919, WO 2005/509479920, WO 2005/092345, WO 2007/119098)
42 book chapters, and 227 oral communications or posters.